Role of Intestinal Microbiota in Ulcerative Colitis

7. Discussion and perspectives
Discussion and conclusion
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7. Discussion and perspectives
7.1. Compositional changes of the fecal microbiota and their capacity to
colonize mucus
The commensal bacteria found in the human gut are important for host health, and maintenance
of tolerance toward the intestinal bacteria by the host is critical to preserve this health. It is
believed that the interaction between host and commensal bacteria is disturbed in UC and this
may have a consequence for the microbiota composition of the gut (Sartor, 2006). Several studies
have previously examined the microbial composition in UC patients and found that it differs from
that of healthy subjects (Ott et al., 2004;Mylonaki et al., 2005;Frank et al., 2007;Takaishi et al.,
2008;Sokol et al., 2009;Qin et al., 2010). Among these studies, only a few have used samples from
both UC patients in remission and relapse for comparison (Mylonaki et al., 2005;Takaishi et al.,
2008;Sokol et al., 2009).
In Paper 1, fecal samples from UC patients in remission or relapse, and healthy subjects were
analyzed by PCR‐DGGE fingerprint and qPCR based principal component analysis (PCA). The results
revealed that UC patients in relapse appeared to have a different fecal microbiota than healthy
subjects and this difference could be ascribed to the Gram‐negative bacteria. A potent stimulator
of inflammation from Gram‐negative bacteria is LPS, hence an altered composition of Gram‐
negative bacteria could add to abnormal LPS signaling enhancing mucosal inflammation in UC.
Adding to this, the overall bacterial changes observed in UC patients in relapse described both in
Paper 1 and in literature (Mylonaki et al., 2005;Takaishi et al., 2008;Sokol et al., 2009) could
further promote intestinal inflammation, since the changed composition of commensal bacteria
may be unable to sufficiently induce regulatory immune responses, hence incapable of
terminating inflammation (Geuking et al., 2011). It should however be noted that the bacterial
changes could be a consequence of intestinal inflammation and not the cause, due to hyper‐
responsiveness of the mucosal immune system towards commensals through mutations and/or
over‐expression of TLRs (De Jager et al., 2007;Frolova et al., 2008;Fuse et al., 2010).
The results from Paper 1 also revealed that some samples from patients in remission resembled
those of patients in relapse, while others resembled those of healthy subjects indicating that the
level of some bacterial groups derived from UC patients in remission is similar to healthy subjects,
while others is similar to UC patients in relapse. This is in accordance with previous